18. #ifad2019 heart lung interactions (aldecoa)
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A neglected topic for way too long, the interest in fluid therapy seems to be quickly rising as the medical community is making a shift from looking at fluids as a mere method of stabilization towards the appreciation of its relevant side effects. Many questions remain to be answered indeed: Is the upgrade from saline 0.9% to balanced crystalloids worth the extra cost? Does HES still have a place in the OR? Do we have to fill the gap left by HES on ICU with crystalloids, other colloids or even albumin? Is it really impossible to avoid fluid overload by using only crystalloids? Is there still a definitive place for human albumin? How do we treat and monitor specific patient populations, like patients with trauma, liver failure, brain edema and right heart failure among others? How do we avoid a one-size-fits-all regimen in perioperative goal-directed therapy? What with the fluids beyond resuscitation? And what do the authors of the big fluid trials do in real life themselves? The 9th International Fluid Academy Day will again be a 1 day concise meeting on all aspects of fluid managament and hemodynamic monitoring in the critically ill. Date: October 26th 2019, 8:00 - 18:00
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18. #ifad2019 heart lung interactions (aldecoa)
- 1. HEART & LUNG INTERACTIONS IN FLUID MANAGEMENT Dr. Cesar Aldecoa M.D., PhD. Servicio de Anestesia y Reanimación Hospital Universitario Rio Hortega. Valladolid Email: cesar.aldecoa@gmail.com
- 2. Dr. Cesar Aldecoa HEART&LUNG INTERACTIONS :AGENDA 1. Heart-Lung Interactions: Concept 2. Heart-Lung Interactions. Spontaneous Breathing 3. Heart-Lung Interactions. Mechanical Ventilation • RV & LV: Interdependece • Venous Return and Mechanical Ventilation • Esophageal Pressure and H&L interactions 4. Evaluation Cardiac Function and Prediction of Fluid Responsiveness using H&L Interactions
- 3. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS: CONCEPT • Spontaneous Ventilation is Exercise • Changes in lung volume alter autonomic tone, pulmonary vascular resistance, compress the heart Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection Alveolar collapse increases pulmonary vasomotor tone via Hypoxic vasoconstriction Recruitment maneuvers without overdistension reduces pulmonary artery pressure • Positive-pressure ventilation increases intrathoracic pressure and increases LV ejection. • Spontenous Ventilation decreases Intrathoracic pressure and decreases LV ejection.
- 4. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS: EFFECT ON PULMONAR ARTERY RESISTANCE
- 5. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. SPONTANEOUS BREATHING Magder S. Ann Transl Med 2018;6(18):34
- 6. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. SPONTANEOUS BREATHING Magder S. Ann Transl Med 2018;6(18):34
- 7. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. SPONTANEOUS BREATHING • Increases isovolumetric part ventricuar contraction • Decrease Volume Ejected • Increases Left Ventricular Overload Magder S. Ann Transl Med 2018;6(18):34
- 8. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. SPONTANEOUS BREATHING • Increases transpulmonary pressure • Can induce veins collapse • Can Increase filling of the left heart (squeezing interalveolar vessels) Magder S. Ann Transl Med 2018;6(18):34
- 9. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION Positive-pressure ventilation: • Increasing Pra during inspiration and decreasing it during expiration. • Increasing ITP (Airway, Pra, pericardial and pleural pressures) • Decreases driving pressure for venous return and RV end- diastolic volume . • Increase Abdominal pressure may increase venous return
- 10. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION Berger D, et al.. Am J Physiol Heart Circ Physiol 2016
- 11. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION
- 12. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION • LV contraction contributes 20–40% of RV systolic pressure • RV contraction contributes 4–10% of LV systolic pressure RV & LV: Interdependece
- 13. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION
- 14. Dr. Cesar Aldecoa Heart-Lung Interactions. Mechanical Ventilation Bennett et al Ann Transl Med 2018;6(18):356
- 15. Dr. Cesar Aldecoa Heart-Lung Interactions. Mechanical Ventilation
- 17. Dr. Cesar Aldecoa ΔPpl = ΔPaw × (EL/Ers) Repesse et al Ann Transl Med 2018;6(18):3
- 18. Dr. Cesar Aldecoa Esophageal Pressure & Heart-Lung Interactions Repesse et al Ann Transl Med 2018;6(18):3
- 19. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. MECHANICAL VENTILATION Gelsen et al. Curr Opin Crit Care 2012 PPV : Sensitivity 88%, Specificity 95% Threshold value 12% Many Limitations Open Chest Low Vt High Frequency Vent Arrhythmias Low Lung compliance Grey Zone 9-13% PPV without contra 17-30% Plethysmographic variability index (PVI) Threshlod 14-17%
- 21. Dr. Cesar Aldecoa Heart-Lung Interactions. Mechanical Ventilation Jozwiak et al . Ann Transl Med 2018
- 22. Dr. Cesar Aldecoa HEART-LUNG INTERACTIONS. • End-expiratory occlusion test. Echocardiography • Increase 5-9% the velocity-time integral of the left ventricular outflow tract. • Added effects of end-expiratory and end-inspiratory occlusion tests increase threshold 13%. • Passive Leg Raising • Surrogates of CO : Peak velocity femoral arteries, CO2 end-Tidal • Spontaneous breathing, atrial fibrilation, low lung compliance • False negatives in Patients with Abdominal pressure>16 mmHg • Dynamic arterial elastance • Eadyn : PPV/SVV ratio • Predict which patients would respond to fluid with an increase in mean arterial pressure • Eadyn of 0.89 sensitivity of 94% and a specificity of 100% • The respiratory systolic variation test (RSVT) • Decrease on arterial pressure afer 3 consecutive mechanical breaths • Independent or Vt • As accurate as PPV and SVV Jozwiak et al . Ann Transl Med 2018 Bennet et al. Ann Transl Med 2018 Monnet et al. Ann. Intensive Care 201
- 23. Dr. Cesar Aldecoa HEART & LUNG INTERACTIONS: LIMITS L.- Low heart rate-to-respiratory rate ratio (HR/RR ratio<3,6) I.- Intra-abdominal hypertension M.- Mechanical ventilation with low tidal volume (Vt < 8ml/kg) (Vt Challenge) I.- Irregular heart rhythm T.- Open Thorax S.- Spontaneous breathing S.T. Vistisen et al. Best Pract & Res Clin Anaes(2019) Jozwiak et al . Ann Transl Med 2018
- 24. Dr. Cesar Aldecoa Jozwiak et al . Ann Transl Med 2018
- 25. Dr. Cesar Aldecoa TAKE HOME MESSAGES • The interactions between ITP and the blood flow through the cardiac chambers during a respiratory cycle (spontaneous and mechanical), provides an opportunity to obtain basic information regarding a patient’s cardiac function • Many invasive and not invasive methods that use this interaction has been used to eventually predict fluid responsiveness. • We do not must forget limitations of tests. • An understanding of the interplay between the cardiac and respiratory systems is also important in the everyday management of critically ill and surgical patients.
- 26. Dr. Cesar Aldecoa MANY THANKS FOR YOUR ATENTION
Editor's Notes
- The heart is a pressure chamber within a pressure chamber Pressure changes within the thoracic cavity during the respiratory cycle affect the pressure systems to the heart and from the heart to the extra-thoracic spaces but do not alter the intrathoracic vascular relationships. The reasons for these differential effects is because flow through the circuit is determined by driving pressures (pressure gradients) within that circuit. The pressure gradient for blood flow is different for the arterial and venous sides of the circulation. Since intrathoracic pressure (ITP) is the surrounding pressure for the heart, right atrial pressure (Pra) relative to right ventricular (RV) filling is best quantified as Pra minus ITP, referred to as transmural (across the wall) pressure. Similarly, left ventricular (LV) ejection pressure is estimates as arterial pressure minus ITP. Clearly, both transmural Pra and transmural LV pressure vary with changes in ITP while neither the upstream venous driving pressure, referred to as mean systemic filling pressure (Pmsf), nor arterial pressure are affected by isolated changes in IT In patients increased work of breathing, initiation of mechanical ventilatory support may improve O2 delivery because the work of breathing is reduced
- Positive pressure ventilation also affects pulmonary artery resistance and hence RV afterload. The relationship between lung stretching and pulmonary artery resistance is U-shaped. Nadir occurs at functional residual capacity and pulmonary artery resistance increases at both lower or higher lung volumes, of which the latter is predominant in positive pressure ventilation [3]. The RV adapts poorly to acutely increased pulmonary artery resistance due to limited contractile reserve, thereby resulting in lower stroke volume (SV)
- Interaction of return and cardiac functions. Bottom left shows the venous reservoir (blue) draining through a resistance to the heart (red) which then pumps the blood back to the venous reservoir. The box indicates the thoracic compartment. The vertical double arrow indicates the pressure difference for venous return (dVR). The top left shows plot of cardiac and return functions. Pra = right atrial pressure and Q = cardiac output and venous return. Ptm-1 is the transmural filling pressure of the RV. The right side shows what happens with a decrease in Ppl. The heart is lowered relative to the venous reservoir (increase vertical double arrow). The cardiac function curve is shifted to the left (dotted line). Ptm increases and so does Q.
- Effect of inspiratory effort on venous return and cardiac output. On the left, right atrial pressure (Pra) falls with inspiration (black boxes). The cardiac function curve shifts to the left and right heart filling increases. On the right, Pra does not fall with inspiration because the heart is functioning on the flat part of the cardiac function curve. On the left there could be a small increase in cardiac output with a volume infusion but not in the example on the right side.
- Effect of a decrease in Ppl on the left ventricular pressure-volume relationship. The decrease in pleural pressure (Ppl) moves the pressure volume loop (P-V) down but does not affect the initial aortic valve opening pressure. This increases the isovolumetric part of ventricular contraction and decreases the volume ejected and increases left ventricular afterload. The end-systolic P-V relationship (Pes) is shifted to the right because of the change in the referencing of the intra-cardiac pressures relative to atmosphere
- Effect of increase in transpulmonary pressure (Ptm) on pulmonary flow. On the left, zone III conditions, lowering Ppl to -5 does not affect pulmonary flow. On the right, when Ppl is lowered to -10, left atrial pressure (Ppla) is less than alveolar pressure (Palv) and pulmonary veins collapse creating a vascular waterfall.
- Schematic representation of the relation between the systemic venous return curve, which remains constant, the left ventricular (LV) function curve which moves with changing intrathoracic pressure (ITP) during breathing. Apneic baseline is shown at “A”. With spontaneous inspiration, ITP decreases so does right atrial pressure but cardiac output increases (“B”), whereas, the opposite occurs with positive-pressure inspiration (“C”). ITP, intrathoracic pressure.
- Airway pressure will raise right atrial pressure and decrease the VRdP and venous return. A standstill pressure may be found at the zero flow intercept of a linear regression between the pressure/flow data pairs. Original data from reference (41). VRdP, venous return driving pressure.
- Spontaneous inspiration, by increasing venous return and RV end-diastolic volume also cause similar though markedly less impressive changes in LV end-diastolic volume over the ventilatory cycle independent of LV filling pressure. Although over a sum of heart beats, mean RV stroke volume should equal mean LV stroke volume, there are impressive beat-to-beat variations caused by the effect of ITP on both ventricles. Under normal conditions, pulmonary vasculature low elastance and high capacitance allows for the pulmonary vasculature to accommodate RV stroke volume variations without much change in pulmonary artery pressure (45). So spontaneous breathing increases RV stroke volume and decreases LV stroke volume, which reverse on exhalation but steady state cardiac output is relatively constant The effects of positive pressure ventilation on LV preload are predominantly mediated by the RV. Decreased RV SV, regardless of cause, transmits into reduced LV preload a few heartbeats later due to pulmonary transit time. Further, if the reduction in RV SV is significant as seen in overt RV failure, its end-diastolic volume increases, which, due to the confinement of both ventricles within the pericardium, will push the interventricular septum leftwards. This reduces LV end-diastolic volume further while elevating LV filling pressure
- Figure 1 Frank-Starling and venous return curves in patients receiving positive pressure ventilation (curve A is a responder, curve B a non-responder). There is an increase in intrathoracic pressure in inspiration. This triggers an increase in RAP. As venous return depends on the gradient between Pmsf and RAP, venous return decreases during inspiration. Note that Pmsf does not change during the respiratory cycle, and the movement across venous return curves implies different Frank-Starling curves, as the changes are isovolaemic. The decrease in venous return in inspiration decreases right ventricular filling and subsequently the output from the right ventricle falls. The effects of this are seen on the left ventricle (and on the arterial pressure) during expiration, due to pulmonary transit time. RAP, the right atrial pressure; Pmsf, mean systemic filling pressure.
- Frank–Starling relationship. The slope of the Frank–Starling curve depends on the ventricular systolic function. Then, one given level of cardiac preload does not help in predicting fluid responsiveness. By contrast, dynamic tests include a preload challenge (either spontaneous, induced by mechanical ventilation or provoked, by passive leg raising, end-expiratory occlusion or fluid infusion). Observing the resulting effects on stroke volume allows for the detection of preload responsiveness. EEO end-expiratory occlusion, PLR passive leg raising
- For the same plateau pressure, Ptp may differ greatly according to EL and ECW: some patients will then be exposed to the consequences of a large increase in Ppl, while others will be exposed to the consequences of an increase in Ptp
- Effects of tidal inflation on right atrial intravascular and transmural pressures. This figure represents the measurements of esophageal pressure (E) and right atrial intravascular pressure (RA) in two different patients under positive pressure ventilation. The transmural pressure of the right atrium defined as esophageal pressure minus RA pressure is materialized by the red arrows. In the first patient (panel A), right atrial transmural pressure decreases during tidal inflation, which illustrates the decrease in venous return due to increased intrathoracic pressure. This effect of tidal inflation is responsible for a fall in right ventricle ejection, leading to a decrease in pulse pressure, named delta-down, because of a preload effect of mechanical ventilation. Conversely, in the second patient (panel B), right atrial transmural pressure increases during tidal inflation, illustrating the systemic congestion secondary to the obstacle to RV ejection. This effect is also responsible for pulse pressure variation (delta-down), but is due to an afterload effect of mechanical ventilation. a, end-expiration; b, end-inspiration. E, esophageal pressure; RA, right atrial intravascular pressure.
- “the tidal volume challenge” (29). They demonstrated that an increase in the absolute value of PPV ≥3.5% induced by a transient increase in tidal volume from 6 to 8 mL/kg for 1 minute could reliably predict the increase in cardiac output in response to a fluid bolus performed at a tidal volume of 6 mL/kg whereas the PPV value obtained at 6 mL/kg tidal volume was unreliable for this purpose (29). Similar results were found for stroke volume variation (SVV) obtained from a contour analysis cardiac output monitor (threshold value: 2.5%) (29)